Repair and pain
Does it bring inflammation down?
Almost always measured as a marker in blood rather than as something a person notices. Worth knowing which one a trial actually moved.
54,269
people in trials
9
human studies
15
compounds, animal or cell only
2
trials found nothing
Measured in people
Ranked by how many people, which is a fact about the evidence and not a judgement about the compound. The one at the top is the most studied, which is not the same as the best. Counts are never added across compounds, because the same person can appear in more than one trial.
- 53,902 people2 human studies
UK Biobank proteomics, 53,026 participants, 13.3 years of follow-up: GDF15 was positively associated with 20 to 24 incident chronic diseases (hazard ratios 1.21 to 3.77) and with multimorbidity, with levels largely explained by renal function, liver function, inflammation and obesity.
Metabolism, 2025 · 53,026 people
876 Swedish men aged 35 to 80 followed up to 14 years: serum GDF15 at entry predicted all-cause mortality with an adjusted odds ratio of 3.38 (95 percent CI 1.38 to 8.26), validated in 324 same-sex twins and independent of telomere length, IL-6 and CRP. An association in a cohort, not an intervention.
Aging Cell, 2010 · 876 people
- 203 people2 human studies1 found nothing
found nothingThe largest and longest diabetes trial here: 192 patients, 40 or 500 mg per day for six months. CRP fell 5.6% and 15.9% versus placebo but not significantly, and there was no significant change in weight, BMI, waist, blood pressure, fasting glucose, HbA1c, insulin, C-peptide, free fatty acids, liver enzymes, uric acid, adiponectin or IL-6. Total cholesterol and triglycerides rose slightly on 500 mg. Subgroups with shorter diabetes duration did show a significant CRP reduction.
Pharmacological Research, 2016 · 192 people
Eleven healthy obese men, randomised double-blind crossover, 150 mg per day for 30 days. Sleeping and resting metabolic rate fell; muscle AMPK was activated with higher SIRT1 and PGC-1alpha protein and improved mitochondrial respiration on a fatty-acid substrate; intrahepatic lipid, circulating glucose, triglycerides, ALT and inflammation markers fell; systolic blood pressure and HOMA improved. The strongest positive mechanistic human result in the literature, in eleven men.
Cell Metabolism, 2011 · 11 people
What people using it report
- Reported interest skews toward biomarkers people cannot feel rather than subjective sensation: posters more often describe checking bloodwork such as lipids, glucose or CRP than describing an energy, mood or cognitive change they noticed day to day.
- 60 people1 human study
60 hypopituitary adults on GH for a mean of 10 years were crossed over to four months of placebo. IGF-1 fell from 168 to 98 micrograms per litre, two quality-of-life domains deteriorated, waist circumference and visceral fat rose, and lipids and C-reactive protein worsened, while insulin sensitivity improved.
Journal of Clinical Endocrinology and Metabolism, 2012 · 60 people
- 42 people1 human study
Single-centre, open-label, prospective randomized controlled trial, April to July 2020: 42 patients received thymalin 10 mg intramuscularly daily for 5 days plus standard care, 50 received standard care. No deaths in either group. Radiological progression in 2 of 42 treated against 5 of 50 controls, with faster falls in IL-6, C-reactive protein and D-dimer.
Stem Cell Reviews and Reports, 2021 · 42 people
- 42 people1 human study1 found nothing
found nothingNCT05038488. 42 adults hospitalised with COVID-19 and acute kidney injury randomised 3:2 to MIB-626 1.0 g or placebo tablets twice daily for 14 days. Blood NAD rose gradually from 16.0 to 25.5 to 42.6 micrograms per millilitre at baseline, day 5 and day 14, and NAD metabolites rose rapidly by day 3. Serum creatinine, cystatin C and serum markers of acute kidney injury did not differ between groups. Serum CRP, IL-6 and TNF alpha and indices of disease severity also did not differ. The authors attribute the absence of clinical effect to the slow rise in NAD and call for studies of parenteral administration. Two authors are employees of Metro International Biotech and a third is a consultant to the company.
FASEB BioAdvances, 2025 · 42 people
- 20 people1 human study
Phase 1b, 20 patients with post-surgical or post-traumatic intraocular inflammation, single subconjunctival dose of 45, 90, 450 or 900 mcg (5 per group). 17 non-serious adverse events judged unrelated to treatment; plasma peptide undetectable in the three lower dose groups. No control group, so the observed fall in inflammation cannot be attributed to the drug. Funding not stated in the abstract.
Journal of Ocular Pharmacology and Therapeutics, 2015 · 20 people
- no headcount stated1 human study
30 participants, sponsor AgelessRx (a telehealth prescriber), active not recruiting. Arms combine rapamycin 2 to 6 mg weekly, metformin 500 mg daily, low-dose naltrexone, intranasal NAD+, topical glutathione and a proprietary supplement; primary endpoints VO2 max, a cognitive composite and an inflammation index. Cannot isolate either drug. No results posted.
ClinicalTrials.gov, 2025 · no headcount in the line
Measured in animals or cells, not yet in people
These are separated from the trials above rather than ranked against them, because they answer a different question. A result in a rat is a real result and a reason somebody ran the study; it is not a measurement of what happens in you. Where the human work is missing, the reason is usually money rather than failure, and that is set out at the bottom of this page.
- 1 preclinical study
Measured in animals or cells
Nanoparticle-delivered KPV accelerated mucosal healing and lowered TNF-alpha in a mouse colitis model.
Molecular Therapy, 2017 · animal
- 1 preclinical study
Measured in animals or cells
A thymulin analogue (PAT) dose-dependently reduced endotoxin-induced hyperalgesia and inflammation in rats.
- 1 preclinical study
Measured in animals or cells
In two mouse colitis models KPV led to earlier recovery, greater body-weight regain, fewer inflammatory infiltrates and lower myeloperoxidase activity in colon tissue. Mouse gut inflammation with KPV given alone; nothing here tests KPV in a blend or in people.
Inflammatory Bowel Diseases, 2008 · animal
- 1 preclinical study
Measured in animals or cells
In THP-1 human monocytes, the Chonluten tripeptide cut TNF release from LPS-stimulated cells and, with the four other Khavinson peptides tested, reduced TNF and IL-6 expression and adhesion to activated endothelium. Cell culture only; the study was run with the Khavinson institute, so it is not independent of the originating research lineage.
International Journal of Molecular Sciences, 2022 · in vitro
- 1 preclinical study
Measured in animals or cells
Reduced inflammation after injury in rats.
Journal of Neurosurgery, 2017 · animal
- 1 preclinical study
Measured in animals or cells
Mouse, physiologically ageing wild-type rather than progeroid. Long-term partial reprogramming regimens produced duration-dependent effects in kidney and skin, with reversion of epigenetic clock measures and reduced inflammation, senescence and stress-response gene expression. The authors make no lifespan extension claim for wild-type mice.
Nature Aging, 2022 · animal
- 1 preclinical study
Measured in animals or cells
Rat. Six epigenetic clocks were developed and validated for rat tissues from 613 tissue samples, with two clocks trained on an additional 1,366 human tissue samples to work across both species. A young porcine plasma fraction treatment more than halved the epigenetic ages of blood, heart and liver tissue in old rats, with a smaller but statistically significant effect in hypothalamus, accompanied by improvements in biochemical, physiological, behavioural and cognitive measures and a shift in immunoglobulin G N-glycosylation from pro- to anti-inflammatory. NIH supported with non-US government funding.
GeroScience, 2024 · animal
- 1 preclinical study
Measured in animals or cells
Mouse, with a human observational component. Plasma from voluntarily running mice infused into sedentary mice reduced baseline neuroinflammatory gene expression and experimentally induced brain inflammation. Proteomics showed a coordinated increase in complement cascade inhibitors including clusterin. Intravenous clusterin bound brain endothelial cells and reduced neuroinflammatory gene expression in acute brain inflammation and Alzheimer models. Separately, patients with cognitive impairment who completed six months of structured exercise had higher plasma clusterin. NIH funded.
Nature, 2021 · animal
- 1 preclinical study
Measured in animals or cells
Mouse atherosclerosis models, with 25-hydroxycholesterol and CH25H expression also measured in human lesions. Macrophage-derived 25-hydroxycholesterol promoted vascular inflammation and lesion remodelling, a harm direction in the same organ system as the aortic stiffness study.
Circulation, 2023 · animal
- 1 preclinical study
Measured in animals or cells
Retinal pigment epithelial cybrid cell lines carrying mitochondria from 5 AMD and 3 normal donors treated with clinical dose equivalents of each drug for 48 hours. AMD cybrids had higher baseline caspase activity; the two drugs produced different patterns of apoptosis, oxidative stress and inflammation gene expression. Cell work only. NIH and foundation funded.
Experimental Eye Research, 2021 · in vitro
- 1 preclinical study
Measured in animals or cells
A mechanistic follow-up asking why these effects are sex-specific, reporting that the reduction in hypothalamic inflammation itself differs by sex. A partial answer rather than a resolution.
Aging Cell, 2017 · animal
- 1 preclinical study
Measured in animals or cells
The founding paper. LINE-1 elements become transcriptionally derepressed during cellular senescence and activate a type I interferon response, triggered by cytoplasmic LINE-1 complementary DNA and blocked by LINE-1 reverse transcriptase inhibitors. Treating aged mice with lamivudine downregulated interferon activation and age-associated inflammation in several tissues. Inflammation endpoints, not survival. The paper carries a published author correction in Nature in 2019, which is a correction and not a retraction.
Nature, 2019 · animal
- 1 preclinical study
Measured in animals or cells
Human cells in culture plus aged mice. Senescent human preadipocytes and HUVECs developed a SASP that was suppressed by JAK-pathway RNAi or JAK inhibitors, and conditioned medium from JAK-inhibitor-treated senescent cells was much less proinflammatory. Giving a JAK inhibitor to aged mice for 10 weeks alleviated adipose and systemic inflammation and enhanced physical function. The authors state their findings are consistent with a possible contribution of senescent cells to age-related frailty and speculate about SASP inhibition; they do not report a human outcome.
Proceedings of the National Academy of Sciences, 2015 · animal
- 1 preclinical study
Measured in animals or cells
Cell culture. The senescence-associated secretory phenotype of chondrocytes was characterised by raised p16, p21 and p53, raised TNF-alpha and IL-1-alpha, and lowered Sirt1. Both the AED peptide and a cartilage polypeptide complex normalised the synthesis of those molecules. Chondrocytes in culture, not joints, and no clinical endpoint was measured.
Advances in Gerontology, 2023 · in vitro
- 1 preclinical study
Measured in animals or cells
Apelin production by contracting muscle falls with age in humans and rodents and associates with exercise benefit in older people (observational). Mice lacking apelin or its receptor showed marked age-related muscle deterioration, and restoring apelin signalling improved muscle function via mitochondrial biogenesis, autophagy, anti-inflammatory pathways and muscle stem cells. The interventions are all in mice; PubMed's phase 3 trial label refers to the embedded human cohort, not to apelin administration. Non-US government funded.
Nature Medicine, 2018 · animal
What people using these actually report
Uncontrolled self-reports, gathered from clinic write-ups, regulatory complaint records and public forums, and reproduced here as written. They are the best guide on this page to what people actually do, what they expect, and what goes wrong, and they cannot show that anything works, because nobody was measured against a placebo and the people who saw no effect mostly stopped posting. Both halves of that are true at once. The negative reports are kept in for the same reason.
- Reported interest skews toward biomarkers people cannot feel rather than subjective sensation: posters more often describe checking bloodwork such as lipids, glucose or CRP than describing an energy, mood or cognitive change they noticed day to day.
Sources: LONGECITY's Resveratrol subforum (including a long-running 'Positive, Negative, ZERO, effect noticed?' poll thread and a dedicated side-effects thread), general web search of longevity-community and vendor commentary on dosing, form and piperine practice, and Peter Attia's public podcast and written statements. Direct access to r/longevity, r/Supplements and r/Biohackers on Reddit was not available in this research pass (Reddit pages could not be fetched and did not surface in general web search here), so those specific subreddits could not be independently checked and any overlap with the sentiment described above is inferred, not confirmed firsthand.
Why the trial record looks like this
A missing trial is usually a missing sponsor. Nobody runs a nine-figure programme on a molecule they cannot own, so the compounds with the thinnest human records are often the oldest and most freely available ones rather than the weakest. Taking KLOW blend as the example, because it states the problem most clearly:
There is no combination trial and there is unlikely to be one. Nobody can patent a four-way mixture of unpatentable peptides, so no sponsor has a reason to fund the study, and the product exists in a market that does not need one to sell. A thin record here is an economic fact about the product category rather than a hidden verdict on any single ingredient. It is still an absence, and it is the absence that matters most: a buyer is not choosing between four studied peptides and one, they are choosing between four separate thin literatures and a mixture that has none.
The copper is the specific thing this page exists to say. At 50 mg of GHK-Cu, about 62.5% of the powder, the vial carries roughly 7.9 mg of elemental copper against a total body copper content of 50 to 120 mg and a dietary upper intake level of 10 mg a day for copper swallowed. Injected copper does not pass the gut, which is where absorption is normally regulated, so the dietary numbers are context and not a limit. Anyone with Wilson's disease, another copper handling disorder, a raised serum copper or a low ceruloplasmin should not go near it, and almost nobody buying a blend has checked. Verify the fraction rather than taking it on faith: PubChem lists copper tripeptide-1 at 402.92 Da and the free tripeptide at 340.38 Da, and the difference is a single copper atom at 63.55, which is 15.8% of the complex.
The fixed ratio deserves its own sentence because it is the part buyers underrate. Every dose decision in this vial was made by the vendor. You cannot raise the BPC-157 without raising the copper by five times as much. You cannot drop the copper when your skin darkens without dropping the peptide you bought the vial for. And when something works or something goes wrong, you have four candidates and no way to tell them apart. A stack of four single-ingredient vials costs more and is more work, and it is the only version of this that can be adjusted or stopped one part at a time.
One more caveat on the arithmetic itself. It assumes the vial contains what the label claims, in the ratio the label claims. Nobody has independently assayed vendor blends, and FDA reviewers examining the single-ingredient version of one of these peptides in 2026 found mislabelled products in the same market.
A compound appears here only when a citation on its own page states this outcome and reports a result for it; naming it is not enough. Human, animal and cell work are counted separately and never merged. Participant counts are read from the study lines and deliberately undercount. Nothing here is advice, and nothing here is a recommendation to take or to avoid anything.